I was particularly fascinated by Ralph's account of the differences in
visual cortex size between Australian indigenes and Whites. The possible
explanations for these differences are questions to be answered. I would not
assume _a prior_ that the differences are necessarily genetic, however. I
wouldn't be surprised if these differences reflected genetic differences, but
neither would I be surprised if they did not. Somatic adaptation, and
particularly organizational levels of somatic adaptation continue to be
largely a black box, although the increasingly sophisticated research focus
on biomechanics is beginning to make it less so.

One of the most original of Gregory Bateson's papers is _The Role of Somatic
Adaptation in Evolution_. Here he is thinking about how somatic adaptations
to specific environmental conditions make those adaptations appear almost
Lamarckian in their replications over generations. Taking the organism as a
hierarchically ordered system, he asks how one might investigate how deeply
in the system an adaptation can be sunk--the genes being the lowest level
(he uses the hydrodynamics of the shark's body as an example of the latter).
The most famous (now infamous) example of this sort of sinking is the case of
the Midwife toad, a dry land toad that developed sitting pads on its thighs
when the experimenter, Phillip Kammerer, placed these toads in a watery, mossy
environment. When the next set of tadpoles appeared, voila, they all had
sitting pads on their legs. Kammerer claimed this as an example of the truth
of Lamarckian inheritance. Sir William Bateson, the villain in Arthur
Koestler's account of the affair, refused even to look at the specimens. We
now understand this case to be an example of genetic assimilation. The
genetic information for developing sitting pads was already there in the toad,
and all it took was the proper environment for the phenotype to express it.

One way to determine whether an adaptation is genetic or somatic was Bateson's
second stress hypothesis. If an adaptation is genetic, then when one
experimentally adds or observes in nature a new sort of stress to the soma,
the animal ought to be able to adapt to it after some time. If the
adaptation in question is somatic, then a new sort of stress should cause
severe damage to the population. The late Geogeda Buckbinder tested this
hypothesis among five groups of Maring in New Guinea living in 5 different
ecozones. She was looking at the body size as an adaptation to dietary
insufficiency. Determining the actual daily calorie intake for each group,
and using blood samples for genetic comparisons between groups, she determined
that there was a statistically significant correlation between calorie intake
and body size with no noticeable differences in gene frequencies among the
5 groups. But there was a new stress in all of these populations--western
introduced diseases, both measles, chicken pox, influenza epidemic diseases,
and chronic diseases such as bronchial illnesses. These diseases had been
introduced 25 years previous to her work. The clearest responses to the
combination of malnutrition and the new stresses was apparent when she
collected information on reproductive histories and population variability.
The groups near the top of the mountain in the poorest producing ecozone
had the lowest live birth rate, well below 2 children per couple. The birth
rates increased gradually as she went down the mountain to richer ecozones,
but only the two groups nearest the valley were reprodicing enough children
to replace the population. The valley group, the best fed but subject to
malaria as well as the new diseases, showed no change in birth rates whatever
over 25 years. She concluded from this evidence that body size was a somatic,
not a genetic adaptation. Her book on the subject, completed in 1975, remains
unpublished.

If it is the case that the direction of the genome's evolution is one of
providing an ever greater flexibility for variable somatic adaptations (see
also Ross Ashby's "Law of Requisite Variety"), then the problems of observing
somatic variability have to do with what cyberneticians call self-organization
of the nervous system, the flexibility of neoronal connections to organize
(transformations of) environmental inputs in any number of patternings. But
the patterns, once formed, are likely to be very stable over time. This sort
of self-organization, now reproducable to some extent in machines, manifests
itself in the observable responses to (often self-selected) environmental
events that we choose to label "intelligent" behavior, personality, and culture
(all thought of as "things" or what Dan Foss likes to call thingies).

Another word that descibes this process of self-organization is "learning to
learn," as discussed not only by Bateson, but by Gordon Pask and, currently,
many others--almost none of them anthropologists (Jim Barnes being an exception
as I read his definition of intelligence). The implication is that once
genetic information completes its circuitry of chemical pathways and gets
transformed into electrical information, the neurons have a wide range of
possible ways of organizing that information and its pathways. This appears
to be true not only for mammals, but for birds and gulls as well, from the
research I've read.

I agree with Harriet and Ralph that the racists will so their thing no matter
what. What we have to worry about is how we organize our thinking about these
data and our research. Looking for thingies in the brain is nothing more than
a couple more millenia of very long, unproductive long days.